Acta Clin Croat 2015; 54:208-215

Professional Paper

ADVERSE DRUG REACTIONS IN THE ORAL CAVITY

Vanja Vuievi Boras1, Ana Andabak-Rogulj2, Vlaho Brailo2, Sonja Kraljevi imunkovi4, Dragana
Gabri3 and Danko Velimir Vrdoljak 5

1
Zagreb University Hospital Center; 2Department of Oral Medicine, 3Department of Oral Surgery, 4Department
of Prosthodontics, School of Dental Medicine, University of Zagreb; 5Clinical Hospital for Tumors,
Sestre milosrdnice University Hospital Center, Zagreb, Croatia

SUMMARY Every medication may lead to adverse effects, even when used in standard doses
and mode of application. In the oral cavity, adverse effects may affect every part of oral mucosa and
are the result of medications taken either locally or systemically. Oral adverse reactions to drugs
are not typical and therefore sometimes not easy to recognize. On diagnosing adverse side effects
in the oral cavity, experienced clinician will usually diagnose the condition on the basis of detailed
medical history and clinical finding. However, the only objective evidence for the offending drug
is re-challenge, i.e. exposure to the drug after its discontinuation. It carries a huge risk of anap-
hylactic reaction; therefore it has to be performed in a controlled hospital setting. Therapy is based
on immediate exclusion of the offending drug and, if lesions are present in the oral cavity, topical or
systemic corticosteroid therapy is prescribed. This article gives a review of patients with oral adverse
drug reactions referred to the Department of Oral Medicine in Zagreb.
Key words: Pharmaceutical preparations adverse effects; Oral manifestations diagnosis; Oral ma-
nifestations therapy

Introduction alivation, burning mouth symptoms, oral ulcerations,

Every medication may lead to adverse effects, even
when used in standard doses and mode of application.
Adverse effects may develop on every organ. In the
oral cavity, adverse effects may affect every part of the
oral mucosa and are the result of medications taken
either locally or systemically. Adverse drug reaction
may develop after the medication has been used once
or after few years of continuous medication use. Oral
adverse reactions to drugs are not typical and there-
fore sometimes not easy to recognize.
Adverse effects of systemic medications may be
numerous, but some that are more frequent are hypos-
Correspondence to: Ana Andabak-Rogulj, DMD, Department of
Oral Medicine, School of Dentistry, Gundulieva 5, HR-10000
Zagreb, Croatia
E-mail: anaandabak@gmail.com
Received November 5, 2013, accepted September 22, 2014
erythema multiforme, gingival hyperplasia, lichenoid
reaction and angioedema1.
Fifteen years ago, we retrospectively retrieved oral
adverse effects of the drugs that patients used and were
referred to our Department. Most frequently, sulfon-
amides such as sulfamethoxazole and trimethoprim
(Sinersul), antibiotics, nonsteroidal anti-inflamma-
tory analgesics (NSAID) and propolis were the medi-
cations that induced oral adverse effects2. At the time,
the same findings (except for propolis) were reported
elsewhere throughout the world.
However, it is interesting to note that this trend is
ever changing as new drugs are marketed and others
are withdrawn. On diagnosing adverse side effects in
the oral cavity, experienced clinician will usually di-
agnose the condition on the basis of detailed medical
history and clinical finding. However, the only objec-
tive evidence for the offending drug is re-challenge,

208 Acta Clin Croat, Vol. 54, No. 2, 2015

Vanja Vuievi Boras et al. Oral adverse drug reactions
i.e. exposure to the drug after its discontinuation. It
carries a huge risk of anaphylactic reaction; therefore
it has to be performed in a controlled hospital setting.
And the last but not the least, it is also considered un-
ethical if the offending drug can be replaced by some
other3,4. In the past, radioallergosorbent test, baso-
phil degranulation test, as well as blastic transforma-
tion tests were performed; however, due to the huge
number of false-positive and false-negative results,
they are not considered accurate3. In certain cases
when patients are taking lots of medications, detec-
tion of the offending drug is not straightforward and
it seems prudent that a drug being already known to
cause adverse effects is more likely to be the offend-
ing one. Therapy is based on immediate exclusion of
the offending drug and, if lesions are present in the
oral cavity, topical or systemic corticosteroid therapy
is prescribed3.
Generally, there are no clinical and histopathologic
presentations alone to relate oral adverse reactions to
any specific medication. Many oral adverse reactions
mimic oral lesions that are also seen in the absence of
medication use5.
It is noteworthy that certain herbal infusions (such
as Calendulla officinalis), herbal products (Tinctura
adstringens), as well as some antiseptic solutions may
lead to oral mucosal damage6. In Croatia, the use of
propolis is quite popular. However, quite frequently
the use of propolis leads to adverse effects in the oral
cavity5,6. Another frequent home medicine for oral
Fig. 1. Oral burn after rinsing with Calendulla officina-
lis, colloid silver and schnapps (source: archives of the De-
partment of Oral Medicine, School of Dental Medicine,
University of Zagreb, Zagreb, Croatia).
Acta Clin Croat, Vol. 54, No. 2, 2015
209
use in Croatia is schnapps. From time to time, we en-
counter chemical burn/sloughing of the oral mucosa
due to this phenomenon. A patient was referred to our
Department due to oral lesions that were provoked by
use of Calendulla officinalis, colloid silver and schnapps
(Fig. 1).
Hyposalivation
It is known that more than 500 drugs may lead
to hyposalivation. The medications which most fre-
quently cause hyposalivation are the ones most com-
monly used, such as antihypertensives and psycho-
tropic drugs. It is known that these groups of drugs
cause dry mouth: antihypertensives, anticholinergics,
antihistamines, benzodiazepines, cytostatics, diuret-
ics, proton pump inhibitors and H2 antagonists,
antipsychotics, antidepressants, hypnotics, opioids,
muscarinic antagonists and alpha receptor agonists,
appetite suppressors, bronchodilators, drugs for HIV
treatment, retinoids, medications for migraine treat-
ment, decongestants, and skeletal muscle relaxants7.
Drugs can cause parasympatholytic activity in several
ways, including competitive inhibition of acetylcho-
line at the parasympathetic ganglia and at the effector
junction. Drugs may also influence parasympathetic
response indirectly via interactions with the sympa-
thetic and central nervous systems8. A patient referred
to our Department with severe hyposalivation due to
drug use is illustrated in Figure 2.
Fig. 2. Severe hyposalivation due to drug use (source: ar-
chives of the Department of Oral Medicine, School of Den-
tal Medicine, University of Zagreb, Zagreb, Croatia).
Vanja Vuievi Boras et al. Oral adverse drug reactions
Table 1. Drug-related oral ulceration
Antihypertensives (nicorandil, captopril, losartan)
Antibiotics (penicillamine, vancomycin)
Anticonvulsants (carbamazepine, phenytoin)
Analgesics (diclofenac, indomethacin)
Alendronate
Allopurinol
Dideoxycytidine
Interferons
Pancreatin
Psychotropics (sertraline, olanzapine)
Burning Mouth Symptoms
Burning mouth symptoms are most frequently lo-
cated on the tongue and are usually a consequence of
using angiotensin converting inhibitors (ACE) such
as lisinopril, captopril, enalapril, etc.9. Burning symp-
toms may develop few days after the medication use
has been initiated, but also they can appear after years
of the drug use. When the offending drug is replaced,
sooner or later burning symptoms will resolve. The
mechanism by which ACE inhibitors can lead to the
burning mouth symptoms remains unknown.
Oral Ulcerations
It is known that NSAIDs and beta blockers may
lead to the development of oral ulceration9,10. Further-
more, sodium lauryl sulfate, which is found in most
toothpastes, in some people can cause lesions that look
Fig. 3. Ulceration due to the use of methotrexate (source: ar-
chives of the Department of Oral Medicine, School of Den-
tal Medicine, University of Zagreb, Zagreb, Croatia).
210 Acta Clin Croat, Vol. 54, No. 2, 2015
Table 2. Drug-related angioedema
ACE inhibitors (captopril, enalapril)
Analgesics (aspirin, ibuprofen, indomethacin,
naproxen)
Antibiotics (penicillamine, penicillin derivatives,
clindamycin, cephalosporins, streptomycin) and co-
trimoxazole, sulfonamides
like ulcers. Mouth ulcers can occur as side effects of
immunosuppressive therapy. Namely, immunosup-
pressants may lead to the activation of herpes virus
or other viruses such as cytomegalovirus, which can
be manifested as oral ulceration. Some drugs, such
as phenylbutazone, can cause agranulocytosis, which
may manifest with oral ulcerations11. NSAIDs may
cause mucosal ulceration due to local vasoconstric-
tion12. Nicorandil induced oral ulcerations are prob-
ably due to its metabolites as the onset of oral ulcer-
ations may occur weeks to months after initiation of
nicorandil therapy. There is large individual variation
in the levels of activity of the enzyme nicotinamide
N-methyltransferase that catalyzes methyl conju-
gation of nicotinamide, an intermediate formed by
denitration of nicorandil13. A few years ago, for the
first time probably, we described a side effect of tak-
ing Spiriva (tiotropium bromide) for the treatment of
chronic obstructive pulmonary disease that occurred
in a patient each time when he inhaled the drug14. The
antimetabolite drug methotrexate may also cause oral
ulcerations (Fig. 3). Table 1 summarizes drugs most
frequently involved in the development of oral ulcer-
ations.
Angioedema
Angioedema may develop after taking many drugs
listed in Table 2. Drug-induced angioedema can be
differentiated into three main categories. Firstly, im-
mediate hypersensitivity reactions to betalactam anti-
biotics constitute the most frequent allergic reactions,
which are IgE-mediated15. Secondly, adverse reactions
to NSAID and aspirin are generally non-allergic, in
which inhibition of cyclooxygenase results in major
alterations in arachidonic acid metabolism such as
cysteinyl leukotriene overproduction15. ACE inhibi-
tors do not mediate angioedema through an allergic
or idiosyncratic reaction; they seem to facilitate an-
Vanja Vuievi Boras et al. Oral adverse drug reactions
gioedema in predisposed individuals. The mechanism
of angioedema with regard to ACE inhibitor therapy
is believed to be related to the kallikrein-kinin plasma
effector system. One hypothesis is that bradykinin,
which is normally degraded by kininase II/ACE, ac-
cumulates in tissues15.
Gingival Hyperplasia
A well known side effect of antihypertensive drugs,
anticonvulsants and cyclosporine is gingival hyperpla-
sia, which usually occurs several months after therapy
with the drug has started. Hyperplasia worsens with a
lack of oral hygiene, so frequent dental check-ups are
recommended. Calcium channel blocker amlodipine,
a medication used to lower blood pressure, can cause
gingival hyperplasia (Fig. 4). Other drugs16-18 can
lead to gingival hyperplasia less frequently and some
are listed in Table 3. Phenytoin has been shown to
induce gingival overgrowth by its interaction with a
subpopulation of sensitive fibroblasts19. Cyclosporine
has been suggested to affect the metabolic function
of fibroblast (e.g., collagen synthesis, breakdown),
whereas nifedipine, which potentiates the effect of cy-
closporine, reduces protein synthesis of fibroblasts20.
Erythema Multiforme
Erythema multiforme (EM) lesions can appear on
the lips, oral mucosa and conjunctiva. Oral manifesta-
tions of EM include bullae and erosions (Fig. 5). The
condition can also affect other mucous membranes.
Fig. 4. Amlodipine induced gingival enlargement (source:
archives of the Department of Oral Medicine, School of
Dental Medicine, University of Zagreb, Zagreb, Croatia).
Acta Clin Croat, Vol. 54, No. 2, 2015 211
Table 3. Drug-related gingival swelling
Antihypertensives (amlodipine, diltiazem, felodipine,
lacidipin, nifedipine, verapamil)
Antimicrobials (erythromycin) and co-trimoxazole
Immunosuppressants (cyclosporin, interferon-alpha)
Psychotropics (lithium, sertraline)
Oral contraceptives
Anticonvulsants (lamotrigine, phenobarbitone,
phenytoin valproate, vigabatrin)
Many drugs21 can lead to the development of EM
and the most common ones are listed in Table 4. The
etiopathogenesis of EM is not completely understood,
but it seems to involve a hypersensitivity reaction to
microbial and chemical agents. It seems that oral mu-
cosa changes correspond to the ones seen in the skin
of people affected with EM. In the beginning, epi-
dermis becomes infiltrated with CD8 T-lymphocytes
and macrophages, whereas the dermis shows slight
Table 4. Drug-related erythema multiforme
Analgesics (acetylsalicylic acid, codeine, diclofenac,
phenylbutazone, piroxicam, tenoxicam)
Anticonvulsants (carbamazepine, hydantoin,
phenytoin)
Antifungals (griseofulvin, fluconazole)
Antihypertensives (amlodipine, digitalis, diltiazem,
nifedipine, verapamil)
Antimicrobials (clindamycin, chloramphenicol,
ethambutol, penicillin derivatives, rifampicin,
streptomycin, tetracyclines, vancomycin), co-
trimoxazole
Diuretics (furosemide, hydrochlorothiazide,
indapamide)
Hormones (minoxidil, mesterolone, progesterone)
Measles/mumps/rubella vaccines
Atropine
Allopurinol, busulfan, fluorouracil
Omeprazole
Retinol
Theophylline
Zidovudine
Vanja Vuievi Boras et al. Oral adverse drug reactions

Lichenoid Reaction
The emergence of oral lichenoid reactions to the
medication has variable latency period that can last
from several weeks to several years from the mo-
ment when the patient started taking the offending
drug. Probably the formation of lichenoid reactions
depends on many factors such as the type, dosage,
previous exposure to the drug, etc. 23. Today, it is
considered that NSAIDs and ACE inhibitors often
lead to lichenoid reactions in the oral cavity24,25. It
Fig. 5. Erythema multiforme after taking Sinersul (sul- is also known that other drugs may induce oral li-
famethoxazole and trimethoprim) (source: archives of the chenoid reactions (Table 5). The most reliable evi-
Department of Oral Medicine, School of Dental Medi- dence is disappearance of lichenoid reaction after
cine, University of Zagreb, Zagreb, Croatia). drug discontinuation and recurrence of lesions after
re-taking the drug, which is often difficult because of
the risk of anaphylactic reaction1. Several years ago,
influx of CD4 lymphocytes. These immunologically
a patient was referred to our Department and had
active cells are not present in sufficient numbers to be
lichenoid reaction to alendronate (Fosamax) (Fig.
directly responsible for epithelial cell death. Instead,
6). The pathogenetic mechanism of lichenoid drug
they release cytokines, which mediate the inflamma-
reaction is incompletely understood. T cells, kerati-
tory reaction and lead to death of epithelial cells22.
nocytes, dendritic cells and endothelial cells, which
express activation markers and adhesion molecules,
Table 5. Drug-related lichenoid reactions are thought to be involved in the inflammatory reac-
tion that ultimately leads to apoptosis of basal kera-
Analgesics (phenylbutazone, piroxicam) tinocytes26.
Antidiabetics (chlorpropamide, metformin,
tolbutamide)
Anticonvulsants (carbamazepine, phenytoin)
Antihypertensives (captopril, flunarizine, labetalol,
methyldopa, oxprenolol, prazosin, procainamide,
propranolol)
Antifungals (griseofulvin, ketoconazole)
Antimalarials (chloroquine, colchicine, dapsone,
hydroxychloroquine, quinine)
Antimicrobials (levamisole, lincomycin,
metronidazole, niridazole, penicillamine, penicillins,
prothionamide, rifampicin, streptomycin,
sulfonamides, tetracycline)
Drugs that act upon the central nervous system
(amiphenazole, barbiturates, chloral hydrate,
cinnarizine, lorazepam, lithium, phenothiazines)
Antiplatelet activity (dipyridamole, phenindione)
Oral contraceptives Fig. 6. Lichenoid reaction to alendronate (Fosamax)
(source: archives of the Department of Oral Medicine,
Protease inhibitors
School of Dental Medicine, University of Zagreb, Zagreb,
BCG, cholera, hepatitis B vaccines Croatia).

212 Acta Clin Croat, Vol. 54, No. 2, 2015

Vanja Vuievi Boras et al. Oral adverse drug reactions

Table 6. Drug-related oral mucosal pigmentation

Analgesics (aminophenazone)
Antihypertensives (methyldopa, propranolol,
quinidine)
Antimicrobials (clofazimine, doxorubicin, doxycycline,
ketoconazole, minocycline)
Antimalarials (chloroquine, hydroxychloroquine)
Antiretrovirals (zidovudine)
Chemotherapeutic agents (busulfan,
cyclophosphamide, fluorouracil)
Fig. 7. Oral mucositis due to 5-fluorouracil (source: ar-
Hormone-replacement therapy, contraceptives, chives of the Department of Oral Medicine, School of
diethylstilbestrol Dental Medicine, University of Zagreb, Zagreb, Croa-
Psychotropic drugs (fluoxetine) tia).

Oral Mucosal Pigmentations Mucositis

Drugs can induce oral mucosal pigmentation.
Most common drugs that induce oral mucosal pig-
mentations are listed in Table 6. Discoloration of oral
mucosa also occurs with intoxication with bismuth
(blue, brown and black), copper (green), bromine,
gold, iron, manganese, lead and silver (gray and blue)1.
The pathogenesis of drug-induced pigmentation de-
pends on the causative drug. It can result from ac-
cumulation of melanin, deposits of the drug or one of
its metabolites. Furthermore, some drugs may induce
synthesis of pigments or iron can be deposited after
damage to the blood vessels27.
Chemotherapeutic agents such as 5-fluorouracil
(Fig. 7), methotrexate, bleomycin, doxorubicin, mel-
phalan and mercaptopurine may lead to the develop-
ment of mucositis28. Mucositis occurs when chemo-
therapy induces breakdown of the rapidly dividing
epithelial cells lining the gastrointestinal tract, leaving
the mucosal tissue open to ulceration and infection.
During the initiation phase, chemotherapeutic agents
lead to the generation of free radicals and DNA dam-
age29.

Fig. 8a and b. Atrophic and pseudomembranous candidiasis as a result of medication use (antibiotics and bronchodila-
tors) (source: archives of the Department of Oral Medicine, School of Dental Medicine, University of Zagreb, Zagreb,
Croatia).

Acta Clin Croat, Vol. 54, No. 2, 2015

213
Vanja Vuievi Boras et al. Oral adverse drug reactions
Candidal Infection
The administration of broad-spectrum antibiot-
ics, corticosteroids, cytotoxic medications and other
immunosuppressants may predispose patients to can-
didal infection due to alterations in commensal oral
microflora30. It is known that oral microflora controls
Candida levels through competition for epithelial
cell adhesion and dietary substrates31. A large num-
ber of drugs that induce xerostomia may also influ-
ence development of candidal infection either in atro-
phic or pseudomembranous forms. Reduction in the
amount of saliva as well as its antimicrobial salivary
constituents (immunoglobulins, lactoferrin, histatins,
lysozyme) may lead to increasing commensal candidal
levels in these patients1 (Fig. 8a and b).
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Saetak

Nuspojave uzimanja lijekova na sluznici usne upljine

V. Vuievi Boras, A. Andabak-Rogulj, V. Brailo, D. Vidovi Juras, D. Gabri, S. Kraljevi imunkovi i D. V. Vrdoljak

Svaki lijek moe imati neeljene nuspojave, ak i kada se koristi u terapijskim dozama i prema propisanom reimu.
Neeljene nuspojave u usnoj upljini mogu se pojaviti na bilo kojem dijelu oralne sluznice i mogu biti posljedica primjene
lijeka lokalnim ili sustavnim putem. Nuspojave lijekova u usnoj upljini nisu specifine i ponekad ih je teko prepoznati.
Prilikom dijagnosticiranja nuspojava lijekova u usnoj upljini iskusni lijenik obino e dijagnosticirati stanje na temelju
detaljne povijesti bolesti i klinikog nalaza. Meutim, jedini objektivni dokaz koji bi upuivao na uzroni lijek je tzv. re-
challenge, odnosno ponovna izloenost lijeku nakon prestanka njegove primjene. S obzirom na to da takav nain testiranja
nosi veliku opasnost od razvoja anafilaktine reakcije treba ga provesti u kontroliranim bolnikim uvjetima. Lijeenje se
temelji na trenutnom prekidu uzimanja uzronog lijeka, a ako su prisutne lezije u usnoj upljini ordinira se lokalna i/ili
sustavna terapija kortikosteroidima. Ovaj pregledni lanak je nastao na temelju prikaza bolesnika koji su upueni na Zavod
za oralnu medicinu u Zagrebu.
Kljune rijei: Farmaceutski pripravci nuspojave; Oralne manifestacije dijagnostika; Oralne manifestacije terapija

Acta Clin Croat, Vol. 54, No. 2, 2015 215